Redox signaling in ischemic postconditioning protection involves PKC ε and Erk1/2 pathways and converges indirectly in Nrf2 activation.

Redox signaling in ischemic postconditioning protection involves PKCε and Erk1/2 pathways and converges indirectly in Nrf2 activation. Cell Signal. 2019 Sep 13;:109417 Authors: Díaz-Ruíz JL, Macías-López A, Alcalá-Vargas F, Guevara-Chávez JG, Mejía-Uribe A, Silva-Palacios A, Zúñiga-Muñoz A, Zazueta C, Buelna-Chontal M Abstract Ischemic-postconditioning (iPostC) exerts cardioprotection by preserving redox homeostasis in the reperfused heart. This protective effect has been associated with the activation of endogenous antioxidant response driven by transcription factor Nrf2 and with the activation of 'reperfusion injury salvage kinases' (RISK) as PI3K, PKC and Erk1/2. Redox homeostasis is essential for normal cell physiology since reactive oxygen species (ROS) are crucial for processes that involve protein signaling. Thus, it has become clear that not only the perturbation of redox balance to oxidative state is deleterious but also towards a reductive state contributing to pathogenesis of diseases. However, there is still a scarce knowledge about the role of ROS in the cardioprotective signals mediated by RISK in postconditioned hearts. Therefore, we studied the role of ROS as initiator of RISK signaling molecules in iPostC-conferred cardioprotection. With the aim to study the relationship between redox-dependent RISK activation and the downstream activation of the transcription factor Nrf2, we evaluated the effect of redox ...
Source: Cellular Signalling - Category: Cytology Authors: Tags: Cell Signal Source Type: research